The poteny of delapril is about 15 times greater than captopril and almost equal to enalaprilat in inhibiting rabbit lung ACE activity in vitro and about 10 times greater than captopril in inhibiting angiotensin I-induced contraction in isolated tissue preparations, such as rat aortic rings and rat kidney[2].

体内研究

After oral administration of [14C]delapril 10 mg/kg to rats, 57% of the dose is absorbed mainly in the small intestine via the portal route and extensively metabolized by esterases to the diacid derivative M-I. Plasma levels of M-I peak within 0.4 hour of administration (maximum concentration [Cmax] 1.23 μg/mL), then decline biphasically with half-lives of 0.6 and 9.1 hours. In dogs given 10 mg/kg of [14C]delapril, 72% of the dose is absorbed. Plasma levels of M-I peak within 0.4 hour of administration (Cmax, 0.9 μg/ mL), then decline biphasically with half-lives of 0.3 and 2.8 hours. Delapril is able to inhibit plasma and tissue ACE at doses 5-10 times lower than captopril and this has also been found in in vivo experiments. Delapril has been shown to decrease heart weight, left ventricular weight, the wall to lumen ratio of small coronary arterioles, and thickness of the left ventricular wall in stroke-prone SHR, to reduce cardiac renin gene expression in SHR, and to protect perfused rat hearts against ischemia-reperfusion injury[2].